癌症研究
免疫原性细胞死亡
免疫系统
免疫疗法
PARP1
结直肠癌
癌症
免疫原性
程序性细胞死亡
免疫检查点
生物
细胞凋亡
免疫学
医学
聚ADP核糖聚合酶
内科学
DNA
聚合酶
生物化学
遗传学
作者
Yaxin Zhang,Huali Li,Yali Zhao,Lingtao Liu,Yi Zhou,Xingyan Pan,Yan-qing Ding,Wenting Liao,Lu Qi,Chengmei Huang,Na Tang
标识
DOI:10.1038/s41420-025-02360-9
摘要
Colorectal cancer (CRC) presents an obstacle to immunotherapy, primarily because most cases are microsatellite stable (MSS) tumors, which are often described as "cold tumors" with limited immunogenicity. Recent studies have indicated that several therapeutic approaches, such as chemotherapy and targeted therapies, can elicit immunogenic cell death (ICD) and stimulate immune responses. However, challenges such as target affinity and in vivo pharmacokinetics limit the efficacy and immune response of current targeted therapies. In this study, we demonstrate that Macrocarpal I is a potent inducer of ICD by activating the PERK/eIF2A/ATF4/CHOP signaling pathway. Furthermore, Macrocarpal I induces apoptosis and ferroptosis, both of which act as triggers for ICD. Mechanistically, Macrocarpal I directly targets TUBB2B and PARP1, disrupting microtubule polymerization and DNA repair processes. Importantly, treatment with Macrocarpal I enhances the anti-tumor immune response and augments responsiveness to anti-PD-1 therapy in an MC38 syngeneic mouse model of CRC.
科研通智能强力驱动
Strongly Powered by AbleSci AI